Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1996-6-11
pubmed:abstractText
Gene expression from the human T-cell leukemia virus type I (HTLV-I) long terminal repeat (LTR) is mediated by three cis-acting regulatory elements known as 21-base pair (bp) repeats in addition to the transactivator protein Tax. Each of the 21-bp repeats contain nucleotide sequences which are homologous to a cAMP response element (CRE) which bind members of the ATF/CREB family of transcription factors. In this study, we investigated whether CREB alone or in the presence of Tax was able to induce DNA structural changes when bound to CRE sites in the HTLV-I 21 bp, the cellular somatostatin promoter, or a hybrid CRE construct comprised of both the somatostatin and 21-bp repeat sequences. Circular permutation analysis indicated that CREB was able to induce DNA flexure upon binding to each of these elements. However, phasing analysis, which is a more sensitive method to determine the degree and orientation of directed DNA bending, demonstrated that CREB induced DNA bending of the HTLV-I 21-bp repeat and the hybrid CRE but not the somatostatin CRE. The addition of Tax did not change CREB-mediated bending of the 21-bp repeat or the hybrid CRE although it markedly increased the amount of CREB bound to each of these DNA elements. These results indicate that sequence motifs flanking the CRE in the 21-bp repeat are critical for inducing DNA structural changes and that these changes are likely important in mediating Tax activation of the HTLV-I LTR.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4781-90
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8617746-Base Composition, pubmed-meshheading:8617746-Base Sequence, pubmed-meshheading:8617746-Binding Sites, pubmed-meshheading:8617746-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:8617746-DNA, Viral, pubmed-meshheading:8617746-Gene Products, tax, pubmed-meshheading:8617746-Human T-lymphotropic virus 1, pubmed-meshheading:8617746-Humans, pubmed-meshheading:8617746-Molecular Sequence Data, pubmed-meshheading:8617746-Mutagenesis, Insertional, pubmed-meshheading:8617746-Mutagenesis, Site-Directed, pubmed-meshheading:8617746-Nucleic Acid Conformation, pubmed-meshheading:8617746-Oligodeoxyribonucleotides, pubmed-meshheading:8617746-Regulatory Sequences, Nucleic Acid, pubmed-meshheading:8617746-Repetitive Sequences, Nucleic Acid, pubmed-meshheading:8617746-Sequence Homology, Nucleic Acid, pubmed-meshheading:8617746-Somatostatin, pubmed-meshheading:8617746-TATA Box
pubmed:year
1996
pubmed:articleTitle
cAMP-response element-binding protein induces directed DNA bending of the HTLV-I 21-base pair repeat.
pubmed:affiliation
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, 75235-8594, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't